Type 1 diabetes (T1D), the autoimmune form of diabetes, results from T cell mediated destruction of insulin producing beta cells within pancreatic islets (1). The disease is dramatically increasing in incidence, doubling in the last two decades, and is predictable by the measurement of antibodies directed against proteins in beta cells (2-4). Despite being predictable, T1D onset cannot be delayed or prevented. Major efforts at disease prevention have been undertaken using preparations of insulin (subcutaneous, oral, and intranasal) to induce tolerance and delay the onset of clinical symptoms (5-7). Measuring insulin-specific T cell responses from the peripheral blood has been a challenging feat, but would allow for assessment of therapeutic response (e.g. converting an inflammatory T cell response (Th1) into a regulatory response), which has been a major obstacle in these trials.
Thus, there exists a need for improved methods of identifying and monitoring T1D-associated T cell responses in individuals, to select and administer individualized therapies to prevent or treat the disease and to efficiently and effectively monitor T1D disease progression after therapies are administered.